EGFR and glioblastoma: Approximately 88% of glioblastoma (GBM) tumors have abnormalities in growth factor signaling, with alterations to the EGFR gene being particularly common and 40% of GBMs harboring EGFR amplifications, activating point mutations in the tyrosine kinase domain or the constitutively active EGFRvIII mutation.1–3 Given the prevalence of EGFR mutations in GBM, the development of therapeutics targeted to these aberrations has received considerable attention.